Current Research
My work integrates across ecological and evolutionary biology using techniques spanning mathematical models to field studies. My current focus explores how changes in host ecology affect the ecology of their infectious diseases, and consequences for both pathogen and host evolution. I apply this to managed apiculture in an effort to assist beekeepers in maintaining viable honeybee populations, and includes nutrition, ecotoxicology, and wider integration with agroecology from the perspective of a pests & pathogens biologist.
My fundamental expertise is in synthesising theoretical and empirical work – ensuring that models capture critical and realistic aspects of biological systems while empirical studies are grounded in quantitatively sound predictions. In doing so we can best address both fundamental and applied challenges in ecology and evolution. I am particularly minded towards ‘two birds one stone’ study systems, where critical insights into fundamental evolutionary ecology can be gained in tandem with informing applied agroecology and conservation. I have a particular interest in social bees, driven by both their exceptional evolutionary and ecological characteristics and for their importance in global agriculture, ecosystem function, and their cultural significance.
Below I give details on some of the specific areas of research I am currently active in.
Illustration by Nina Sokolov (2019)
Evolutionary Ecology of Honeybee Parasites
A research apiary belonging to the UGA bee lab - North GA 2018
As research in honeybee parasites only grows, there is abundant opportunity to both test fundamental evolutionary-ecological theory and holds promise for immediate, impactful applied science. Much of my work sits at this nexus of understanding the evolutionary ecology of honeybee parasites both as an applied science in improving bee health and as a test system for fundamental evo-eco theory.
One holistic ecological change in beekeeping in the United States is the move towards industrialised beekeeping practices, changing much of managed honeybee ecology. I have undertaken both empirical and theoretical work examining the consequences of this ecological management shift. For example, recent theory (from me) has shown that the packing together of honeybee colonies at high densities means little for the epidemic spread of pathogens. However, further empirical work I undertook tied management background to viral titres in colonies, overall pointing towards severity of infection, not infection alone per se, being a critical component of insect-virus interactions.
These concepts around the impacts of changing host ecology extend to the evolution of parasites in the system. Current work of mine is concluding five years of examining the putative evolution of viruses and their alleged vector the Varroa mite, and consequences for virulence and transmission. This includes conceptual reviews and large field experiments, with results due out shortly beginning to understand the evolutionary forces at play in honeybee health and population declines here and worldwide, more recently including the evolution of resistance to pesticides.
Honeybee Defenses Against Parasites and Pesticides
Honeybees live at extremely high densities and must defend themselves, each other, and their abundant communal resources from exploitation by parasites. The mechanisms by which they do this are evolutionary interesting as well as targets for intentional fortification in applied ecology. Understanding the mechanisms by which honeybees defend themselves is a newer research horizon for me, linking honeybee health to wider bee health through reducing spillover severity.
Genetic diversity within populations helps reduce the severity of epidemics, but in honeybees intracolony diversity also allows for individuals to specialise in specific tasks. Rare genotypes may behave conceptually as colony leukocytes, investing heavily in colony sanitation at multiple levels. Current collaborative work is underway examining how manipulating colony diversity through both queen insemination and intercolony brood transplantation may allow honeybees to better mitigate parasite and pesticide pressures.
One notable mechanism of collective social immunity in honeybee colonies is the deployment of hydrogen peroxide in honey as an antimicrobial agent. Recent collaborative work has shown how honeybee artificial diets differ in their suitability as peroxidase substrates, and that higher peroxide concentrations better defend against a colony parasite, the small hive beetle. Future research plans are afoot to interrogate this costly investment in social immunity and further tie its applied role to work showing the impact of botanical provision in the landscape in peroxide-mediated honeybee defense.
Certain honeybee populations may have recently evolved novel mechanisms of defense against parasites and pathogens, leading to honeybees that are tolerant of specific viruses. Collaborative work is underway conceptualising the potential future ecological consequences of movements in beekeeping chasing virus-tolerant phenotypes, particularly with respect to spillover of honeybee viruses into wild bee populations.
Inner hive cover of a neglected honeybee colony, unfortunately succumbed to an Aethina tumida infestation:- the ‘small hive beetle’ (see white grubs) - Athens GA 2020
Contributions & Consequences in Varroa Control
A trainee beekeeper inspects a colony for parasitic Varroa mites and overall vitality - Young Harris GA 2017
Parasitic Varroa mites remain one of the most insidious problems for beekeeping in the United States and elsewhere. Efforts to develop novel control methods are widespread if challenging, and the consequences of those control methods are often poorly understood despite widespread focus on pesticides and honeybees.
I am currently collaborating on a large project, including the EPA and USDA, trialling in the lab and field candidate novel miticidal agents for Varroa control. This includes examining alternative application methods of current pesticides for effectiveness and consequences for honeybee colony health and likely resistance evolution in the Varroa mites; our work specifically includes current amitraz and oxalic acid applications.
One success story was the eradication of Varroa mites from honeybee colonies on the island of Exuma (Bahamas) following aggressive oxalic acid application and beekeeper training on the island. My collaborations with The Exuma Foundation continue, examining the virological consequences of the removal of this parasitic vector, and what this may also mean for the spillover of viruses into native bees on this island in comparison to elsewhere.
Integrating Reproduction and Spatial Structure in Virulence Evolution
Many evolutionary models assume a mean field population of perfect mixing between individuals; in reality, we know individuals associate with each other heterogeneously, most obviously because of spatial proximity.
This spatial structuring of populations limits virulence evolution, selecting for a lower optimum virulence due to ‘self shading’, whereby infected individuals are more likely to be associated or clustered with other infected hosts (shade) where clustered infected individuals are often hosts to the same pathogen strain (self).
My work on this topic builds on understanding how host-pathogen demographic factors determine the strength of this spatial limiting of virulence. In particular, the role of castration by pathogens both as a consequence of proximate virulence mechanisms and as an alternative strategy to mortality-inducing pathology. I have demonstrated that a previously documented ‘virulence hump’ relies on rare demographic assumptions around host reproductions, with current work to systematically overview which demographic factors predispose spatial structuring to stronger or weaker limitation of pathogen virulence.
Seminar on virulence theory - Tara Beekeepers Seminar GA 2019
Evolution in a Model Insect-Virus System
A rogue male Plodia larva intrepidly marches across a delightfully clean lab bench - U.C. Berkeley 2016
How hosts evolve resistance to their natural enemies, including their parasites, is a rich field of evolutionary theory. From first principles and observing susceptible hosts in nature we can deduce that there must be costs to resistance, but demonstrating and characterising these evolutionary trade-offs is empirically challenging, especially in a manner suitable for direct application to theory.
During my PhD work on the Plodia system, a small moth vulnerable to lethal infection by a specific granulosis virus, I used inbreeding experiments as well as classic selection experiments to show that a trade-off in this systems between host development time and resistance to a pathogen is both constitutive and genetic - a rare demonstration of assumptions made in much of the theoretical literature on host evolution. However I also showed that selecting on development time is not symmetrical with selection for resistance, yielding different evolutionary outcomes despite this apparently tight trade-off.
Current collaborative work in this system continues, including on the context-dependence of how resistance may evolve, as well as the ability of pathogens to specialise on specific host strains with different resistances and plausibly resistance mechanisms.